South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
exacerbating cardiac arrhythmias. Thus, dopamine is no longer a recommended treatment and has
been replaced by dopamine type 1 receptor agonists (e.g., fenoldopam) with more specific effects
on renal arterioles and less adverse effects. In horses, oliguria should progress to polyuria within
48-72 hours after development of ARF for the prognosis for recovery to remain reasonable.
Fortunately, the majority of horses with ARF are nonoliguric rather than oliguric and
administration of furosemide or mannitol is not needed with nonoliguric ARF. When oliguria
persists for more than 72 h, the prognosis becomes grave and peritoneal dialysis may be attempted
but pursuit of this treatment should likely only be offered to clients that want to pursue all
treatments as an alternative to euthanasia.
After volume deficits have been restored and polyuria has been achieved, patients usually only
require continued fluid therapy to promote a continued decrease in Cr. During the week after fluid
therapy is discontinued, Cr should be measured again to ensure that it has not increased.
Occasionally, Cr may not decrease below the uppe r limit of the reference range despite fluid
therapy. As long as the horse is eating and drinking well, IV fluids can be discontinued. In some
horses Cr may return to the normal range over the next couple of months while in other patients a
persisting elevation in Cr is indicative of a permanent loss of renal function.
Chronic kidney disease: A similar change in terminology has been adopted in human and small
animal medicine for patients with chronic renal disease. Rather than describing patients as have
chronic renal failure (CRF, often an end stage problem), the term chronic kidney disease (CKD)
has been introduced to shift attention to detection of earlier stages of chronic renal disease.
Although CKD is by nature a progressive disorder, early detection and interventions may slow the
rate of progression thereby prolonging life and, for people, delaying the potential need for renal
replacement therapy.
CKD in the horse may be divided by clinical and pathologic findings into two broad categories:
primary glomerular disease (glomerulonephritis) and primary tubulointerstitial disease (chronic
interstitial nephritis). However, pathology in one portion of the nephron usually leads to altered
function and eventual pathology in the entire nephron such that CKD is an irreversible disease
process characterized by a progressive decline in GFR. However, the rate of decline in GFR is
variable making the short-term (months to a couple of years) prognosis guarded to favourable
while the long-term prognosis remains poor. Unfortunately, because renal disease is often
advanced when horses are first presented for clinical evaluation, the inciting cause leading to
CKD may be difficult to ascertain, and end stage kidney disease (ESKD) may be the pathologic
diagnosis.
Clinical signs and laboratory findings: The most common clinical sign observed in horses with
CKD is weight loss. A small plaque of ventral oedema, usually between the forelimbs, is another
frequent finding. Moderate polyuria and polydipsia (PU/PD) are also usually present at some
stage of the disease process. Often, urine produced by horses with CKD is light yellow in color
and transparent as it is relatively devoid of normal crystals and mucus. Accumulation of dental
tartar, especially on the incisors and canine teeth, gingivitis, and oral ulcers are other findings that
may be detected in horses with CKD. Decreased performance may be an early complaint in
competitive horses while growth may be stunted in young horses with renal hypoplasia or
dysplasia.
Laboratory findings in horses with CRF vary depending on diet and the cause and extent of renal
damage. Most horses with clinical signs of CRF have moderate to severe azotaemia (Cr usually 5
mg/dl [440 µmol/L] or greater). The BUN to Cr ratio may vary, depending on protein intake,
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